Saturday, August 28, 2010

Insulin is a hormone that drives glucose and other nutrients from the bloodstream into cells, among other things. A loss of sensitivity to the insulin signal, called insulin resistance, is a core feature of modern metabolic dysfunction and can lead to type II diabetes and other health problems. Insulin resistance affects a large percentage of people in affluent nations, in fact the majority of people in some places. What causes insulin resistance? Researchers have been trying to figure this out for decades.*

Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).

The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another common concept in the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fatness (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.

All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).

A large new study just published in the American Journal of Clinical nutrition has taken the evidence to a new level (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:

High saturated fat, high glycemic index

High monounsaturated fat, high glycemic index

High monounsaturated fat, low glycemic index

Low fat, high glycemic index

Low fat, low glycemic index

Compliance to the diets was pretty good. From the nature of the study design, I suspect the authors were expecting participants on diet #1 to fare the worst. They were eating a deadly combination of saturated fat and high glycemic carbohydrate! Well to their dismay, there were no differences in insulin sensitivity between groups at 6 months. Blood pressure also didn't differ between groups, although the low-fat groups lost more weight than the monounsaturated fat groups. The investigators didn't attempt to determine whether the weight loss was fat, lean mass or both. The low-fat groups also saw an increase in the microalbumin:creatinine ratio compared to other groups, indicating a possible deterioration of kidney function.

In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.

Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations may be limited by reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!

Thursday, August 19, 2010

Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.

The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:

Diets 1 and 2 resulted in similar lipids, while diet 3 resulted in lower LDL and higher HDL. A second study also showed that diet 3 resulted in lower oxidized LDL, a dominant heart disease risk factor (2). Overall, these papers showed that freshly pressed virgin coconut oil, with its full complement of "minor constituents"*, partially protects rats against the harmful effects of cholesterol overfeeding. These are the only papers I could find on the cardiovascular effects of unrefined coconut oil in animals!

Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.

In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.

What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.Heart Disease: Human Studies

It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.

Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.

Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).

Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.

Coconut Oil and Body Fat

In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.

Coconut Oil and Cancer

Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.

The Bottom Line

There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.

* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.

Wednesday, August 18, 2010

Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:

Most palms begin to produce nuts about five years after germination and continue to yield them for forty to sixty years at a continuous (i.e., nonseasonal) rate, producing about fifty nuts a year. The immature nut contains a tangy liquid that in time transforms into a layer of hard, white flesh on the inner surface of the shell and, somewhat later, a spongy mass of embryo in the nut's cavity. The liquid of the immature nut was often drunk, and the spongy embryo of the mature nut often eaten, raw or cooked, but most nuts used for food were harvested after the meat had been deposited and before the embryo had begun to form...

After the nut had been split, the most common method of extracting its hardened flesh was by scraping it out of the shell with a saw-toothed tool of wood, shell, or stone, usually lashed to a three-footed stand. The shredded meat was then eaten either raw or mixed with some starchy food and then cooked, or had its oily cream extracted, by some form of squeezing, for cooking with other foods or for cosmetic or medical uses...

Those Polynesians fortunate enough to have coconut palms utilized their components not only for drink and food-- in some places the most important, indeed life-supporting food-- but also for building-frames, thatch, screens, caulking material, containers, matting, cordage, weapons, armor, cosmetics, medicine, etc.

Mainstream Ire

Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.

Coconut Eaters

As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.

One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.

Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).

Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.

The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).

Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.

* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.

Thursday, August 12, 2010

The title of this post is the exact title of a recent editorial in the American Journal of Cardiology (1). Investigators calculated the "risk for cardiovascular disease associated with the total fat and trans fat content of fast foods", and compared it to the "risk decrease provided by daily statin consumption". Here's what they found:

The risk reduction associated with the daily consumption of most statins, with the exception of pravastatin, is more powerful than the risk increase caused by the daily extra fat intake associated with a 7-oz hamburger (Quarter Pounder®) with cheese and a small milkshake. In conclusion, statin therapy can neutralize the cardiovascular risk caused by harmful diet choices.

Wow. Later in the editorial, they recommend "a new and protective packet, “MacStatin,” which could be sprinkled onto a Quarter Pounder or into a milkshake." I'm not making this up!

I can't be sure, but I think there's a pretty good chance the authors were being facetious in this editorial, in which case I think a) it's hilarious, b) most people aren't going to get the joke. If they are joking, the editorial is designed to shine a light on the sad state of mainstream preventive healthcare. Rather than trying to educate people and change the deadly industrial food system, which is at the root of a constellation of health problems, many people think it's acceptable to partially correct one health risk by tinkering with the human metabolism using drugs. To be fair, most people aren't willing to change their diet and lifestyle habits (and perhaps for some it's even too late), so frustrated physicians prescribe drugs to mitigate the risk. I accept that. But if our society is really committed to its own health and well-being, we'll remove the artificial incentives that favor industrial food, and educate children from a young age on how to eat well.

I think one of the main challenges we face is that our current system is immensely lucrative for powerful financial interests. Industrial agriculture lines the pockets of a few large farmers and executives (while smaller farmers go broke and get bought out), industrial food processing concentrates profit among a handful of mega-manufacturers, and then people who are made ill by the resulting food spend an exorbitant amount of money on increasingly sophisticated (and expensive) healthcare. It's a system that effectively milks US citizens for a huge amount of money, and keeps the economy rolling at the expense of the average person's well-being. All of these groups have powerful lobbies that ensure the continuity of the current system. Litigation isn't the main reason our healthcare is so expensive in the US; high levels of chronic disease, expensive new technology, a "kitchen sink" treatment approach, and inefficient private companies are the real reasons.

If the editorial is serious, there are so many things wrong with it I don't even know where to begin. Here are a few problems:

They assume the risk of heart attack conveyed by eating fast food is due to its total and trans fat content, which is simplistic. To support that supposition, they cite one study: the Health Professionals Follow-up Study (2). This is one of the best diet-health observational studies conducted to date. The authors of the editorial appear not to have read the study carefully, because it found no association between total or saturated fat intake and heart attack risk, when adjusted for confounding variables. The number they quoted (relative risk = 1.23) was before adjustment for fiber intake (relative risk = 1.02 after adjustment), and in any case, it was not statistically significant even before adjustment. How did that get past peer review? Answer: reviewers aren't critical of hypotheses they like.

Statins mostly work in middle-aged men, and reduce the risk of heart attack by about one quarter. The authors excluded several recent unsupportive trials from their analysis. Dr. Michel de Lorgeril reviewed these trials recently (3). For these reasons, adding a statin to fast food would probably have a negligible effect on the heart attack risk of the general population.

"Statins rarely cause negative side effects." BS. Of the half dozen people I know who have gone on statins, all of them have had some kind of negative side effect, two of them unpleasant enough that they discontinued treatment against their doctor's wishes. Several of them who remained on statins are unlikely to benefit because of their demographic, yet they remain on statins on their doctors' advice.

Industrial food is probably the main contributor to heart attack risk. Cultures that don't eat industrial food are almost totally free of heart attacks, as demonstrated by a variety of high-quality studies (4, 5, 6, 7, 8, 9). No drug can replicate that, not even close.

I have an alternative proposal. Rather than giving people statins along with their Big Mac, why don't we change the incentive structure that artificially favors the Big Mac, french fries and soft drink? If it weren't for corn, soybean and wheat subsidies, fast food wouldn't be so cheap. Neither would any other processed food. Fresh, whole food would be price competitive with industrial food, particularly if we applied the grain subsidies to more wholesome foods. Grass-fed beef and dairy would cost the same as grain-fed. I'm no economist, so I don't know how realistic this really is. However, my central point still stands: we can change the incentive structure so that it no longer artificially favors industrial food. That will require that the American public get fed up and finally butt heads with special interest groups.

Thursday, August 5, 2010

The American Journal of Clinical Nutrition just published the results of a major Japanese study on saturated fat intake and cardiovascular disease (1). Investigators measured dietary habits, then followed 58,453 men and women for 14.1 years. They found that people who ate the most saturated fat had the same heart attack risk as those who ate the least*. Furthermore, people who ate the most saturated fat had a lower risk of stroke than those who ate the least. It's notable that stroke is a larger public health threat in Japan than heart attacks.

This is broadly consistent with the rest of the observational studies examining saturated fat intake and cardiovascular disease risk. A recent review paper by Dr. Ronald Krauss's group summed up what is obvious to any unbiased person who is familiar with the literature, that saturated fat consumption doesn't associate with heart attack risk (2). In a series of editorials, some of his colleagues attempted to discredit and intimidate him after its publication (3, 4). No meta-analysis is perfect, but their criticisms were largely unfounded (5, 6).

*Actually, people who ate the most saturated fat had a lower risk but it wasn't statistically significant.

About Me

I'm a writer and science consultant with a background in neuroscience and obesity research. I have a BS in biochemistry and a PhD in neurobiology. I'm the author of "The Hungry Brain: Outsmarting the Instincts That Make Us Overeat".

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Disclaimer

This blog is a compilation of my opinions. It's not advice; it's information that you can take or leave as you please. I don't intend it to replace professional medical consultation or treatment. Your health is in your own hands.